Studies on organ development have focused on fetal and neonatal lung as related to the respiratory distress syndrome (RDS). Fetal lung lecithin concentration and the isotopically-measured rate of lecithin synthesis have been shown to increase during the latter 10-20% of gestation in rabbits, rats, and monkeys. The principal pathway for lung lecithin synthesis was found to be the choline incorporation route (I) rather than phosphatidylethanolamine methylation (II) as claimed by others. The use of techniques that permit (by amniotic fluid phospholipid analysis) prenatal identification of infants at high risk for RDS has indicated that these methods provide a specific and direct index of the state of fetal lung maturity in primates. Tissue slice experiments with lungs from term fetal rats and studies with fetal Rhesus monkeys in situ have shown that the choline pathway is inhibited markedly in the presence of pH values less than 7.4. Administration of corticosteroids to the fetus has been found to enhance the rate of lung synthesis within six hours after injection and increases the activity of choline phosphotransferase (CPT). Corticosterone deficient rat fetuses show low lung CPT activity and lecithin synthesis via choline incorporation; this may be increased to normal within six hours after a physiological dose of dexamethasone. In developing fetal rat lung, enhanced choline pathway enzyme activities have been shown to develop within 24 hours after the normal prenatal elevation in fetal plasma corticosterone. Thus, adrenocorticoids may provide the physiologic stimulus for fetal pulmonary maturation. Promising data from clinical trials elsewhere suggest that these agents may be useful in the prevention of RDS.